al-Bayati M A, Culbertson M R, Schreider J P, Rosenblatt L S, Raabe O G
Institute of Toxicology and Environmental Health, School of Veterinary Medicine, University of California, Davis 95616.
J Environ Pathol Toxicol Oncol. 1992 Mar-Apr;11(2):19-27.
The acute toxicity of ammonium metavanadate (15.5 mg/kg) in mice was investigated to examine the induction of lymphoid necrosis to (1) verify the reproducibility of the lesions in the thymus, lymph nodes, and spleen; (2) determine whether the necrosis of lymphoid tissue previously observed during the first 3 days post-treatment but absent at 14 days was the result of differences in sensitivity of the mice or the result of recovery from the effects of vanadium; and (3) determine whether differences in the presence and the degree of necrosis between thymus and spleen were correlated with differences in the uptake of vanadium in these tissues. A timed sacrificed study was conducted in conjunction with a 48V tracer. In this study, BALB/C mice were injected subcutaneously (s.c.) with ammonium metavanadate solution (15.5 mg/kg). Groups of mice were sacrificed at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 21, and 28 days postexposure. Lymphoid necrosis was found in the thymus, spleen, lymph nodes, and bone marrow, with the necrosis being most severe in the thymus. The necrosis was moderate at 0.5 days, most severe at 2 to 3 days, with recovery beginning at 4 days, and proceeding to full recovery at 14 to 28 days. At 0.5 days post-treatment, the concentration of vanadium in thymus and spleen was 4.4 and 8.3 micrograms/g, respectively. At all post-treatment periods, with the exception of the 1- and the 4-day periods, the concentration of vanadium in spleen was significantly higher than in the thymus, p less than 0.05. The treated animals showed neurological signs (ataxia, convulsion, dyspnea, and paralysis of hind legs) between 5 min and 54 hr post-treatment, but the concentration of vanadium in the brain was very low during this period (less than 5.2% of blood concentration).
对偏钒酸铵（15.5毫克/千克）在小鼠中的急性毒性进行了研究，以检查淋巴样坏死的诱导情况，从而（1）验证胸腺、淋巴结和脾脏中病变的可重复性；（2）确定治疗后第1天至第3天观察到但在第14天不存在的淋巴样组织坏死是小鼠敏感性差异的结果还是钒作用恢复的结果；以及（3）确定胸腺和脾脏中坏死的存在和程度差异是否与这些组织中钒摄取的差异相关。结合48V示踪剂进行了定时处死研究。在本研究中，将BALB/C小鼠皮下注射（s.c.）偏钒酸铵溶液（15.5毫克/千克）。在暴露后0.5、1、2、3、4、6、8、10、12、14、21和28天处死小鼠组。在胸腺、脾脏、淋巴结和骨髓中发现了淋巴样坏死，其中胸腺中的坏死最为严重。坏死在0.5天时为中度，在2至3天时最为严重，从4天开始恢复，并在14至28天完全恢复。治疗后0.5天时，胸腺和脾脏中钒的浓度分别为4.4和8.3微克/克。在所有治疗后的时间段中，除了第1天和第4天，脾脏中钒的浓度显著高于胸腺，p小于0.05。治疗后的动物在治疗后5分钟至54小时之间出现神经体征（共济失调、抽搐、呼吸困难和后腿麻痹），但在此期间大脑中钒的浓度非常低（低于血液浓度的5.2%）。
